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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
Advanced glycation end-products and the kidney
Martin Busch1, Sybille Franke, Christiane Rüster
1Department of Internal Medicine III, Jena University Hospital - Friedrich Schiller University, Jena, Germany.
European Journal of Clinical Investigation
|July 24, 2010
Summary
Advanced glycation end-products (AGEs) contribute to kidney and vascular diseases. Circulating AGEs may not reliably predict cardiovascular risk in chronic kidney disease patients.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Endocrinology
Background:
- Advanced glycation end-products (AGEs) accumulate in hyperglycemia and oxidative stress, common in diabetes mellitus.
- AGEs form from nonenzymatic glycation and oxidation of proteins and lipids.
- The kidney is crucial for AGEs clearance and metabolism.
Purpose of the Study:
- To review the role of AGEs and their receptors in kidney and vascular diseases.
- To assess the utility of circulating AGEs as biomarkers for cardiovascular risk.
Main Methods:
- Comprehensive literature search of Medline and other databases.
- Inclusion of key review articles and original research from the authors' group.
Main Results:
- Kidney podocytes and endothelial cells possess AGE receptors, mediating pathophysiological effects like hypertrophy, apoptosis, and inflammation.
- AGEs are implicated in diabetic nephropathy, microvascular complications, other renal diseases, and atherosclerosis.
- Serum AGE levels do not consistently correlate with cardiovascular events in chronic kidney disease (CKD), likely due to poor correlation with tissue-deposited AGEs.
Conclusions:
- AGEs and their receptors are integral to the pathogenesis of vascular and kidney diseases.
- The predictive value of circulating AGEs for cardiovascular risk in CKD is uncertain.
- The therapeutic potential of AGE inhibitors requires further investigation.
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